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2015 ; 278
(5
): 494-506
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Pathogenic immunity in systemic lupus erythematosus and atherosclerosis: common
mechanisms and possible targets for intervention
#MMPMID25720452
Wigren M
; Nilsson J
; Kaplan MJ
J Intern Med
2015[Nov]; 278
(5
): 494-506
PMID25720452
show ga
Systemic lupus erythematosus (SLE) is an autoimmune disorder that primarily
affects young women and is characterized by inflammation in several organs
including kidneys, skin, joints, blood and nervous system. Abnormal immune
cellular and humoral responses play important roles in the development of the
disease process. Impaired clearance of apoptotic material is a key factor
contributing to the activation of self-reactive immune cells. The incidence of
atherosclerotic cardiovascular disease (CVD) is increased up to 50-fold in
patients with SLE compared to age- and gender-matched controls, and this can only
partly be explained by traditional risk factors for CVD. Currently, there is no
effective treatment to prevent CVD complications in SLE. Traditional preventive
CVD therapies have not been found to significantly lower the incidence of CVD in
SLE; therefore, there is a need for novel treatment strategies and increased
understanding of the mechanisms involved in the pathogenesis of CVD complications
in SLE. The pathogenic immune responses in SLE and development of atherosclerotic
plaques share some characteristics, such as impaired efferocytosis and skewed
T-cell activation, suggesting the possibility of identifying novel targets for
intervention. As novel immune-based therapies for CVD are being developed, it is
possible that some of these may be effective for the prevention of CVD and for
immunomodulation in SLE. However, further understanding of the mechanisms leading
to an increased prevalence of cardiovascular events in SLE is critical for the
development of such therapies.
|*Atherosclerosis/etiology/immunology/pathology/prevention & control
[MESH]